How targeting tubular cell metabolism could halt chronic kidney disease
Around 10% of the world’s population is thought to be affected by chronic kidney disease (CKD). Professor Sophie de Seigneux believes that understanding how patients with acute kidney injury (AKI) go on to develop CKD could be a vital step in reducing this burden.
She says: “There are currently very few treatments that are able to slow the progression of CKD. At present, we have ACE inhibitors, RAS blockers, and now SGLT2 inhibitors. So, if we can find something different that can reverse lesions in the kidney, it could dramatically change the prognosis for patients in the long-term.”
Based at Geneva University Hospital in Switzerland, Prof. de Seigneux studies the pathophysiology of kidney disease and, in particular, examines the role of metabolism and mitochondrial function in kidney tubular cells in acute and chronic kidney diseases.
She continues: “Research has shown that in all types of renal disease, we find mitochondrial damage and changes to cell metabolism, and this process seems to predict the deterioration of renal function. This means that, theoretically, we can target this process to halt the disease. The ultimate aim is, of course, to find a new avenue for the general treatment of a wide range of AKIs and CKDs.”
In her talk at WCN’21, Prof. de Seigneux will explain the changes in metabolism and mitochondrial function that occur during acute and chronic kidney disease with reference to her own research and that of others. She will also talk about therapeutic perspectives that have been tested or are being tested in this field, highlighting the most promising treatments.
“These include NAD donors, that my group has worked on, and the synthetic peptide SS31, which other groups have studied. Of course, we look forward to seeing further results of clinical research in the near future. In the meantime, my colleagues and I continue to look for different ways of targeting this process.”
Prof. de Seigneux concludes: “One of the most exciting findings in this field is that targeting metabolism and mitochondrial function in tubular cells could work even after kidney damage has occurred, which is very important in preventing the progression from AKI to CKD.”
Prof. Sophie de Seigneux, “Preventing the progression of AKI to CKD: Role of the mitochondria,” Theme Symposium: Pathophysiology of AKI to CKD. Joint session with ASN, Friday 16 April, 09:30-10:30 hrs Montréal (Canada) time: